Search Results (266)

Mesothelioma is a rare and aggressive malignancy arising from mesothelial cells. Despite recent advances in systemic therapies, overall survival remains limited, underscoring the need for a deeper mechanistic understanding of disease pathogenesis and novel therapeutic strategies. In mesothelioma, chronic tissue injury induced by asbestos fibers leads to sustained activation of innate immune pathways and chronic inflammation that actively promote tumorigenesis. The release of Damage-Associated Molecular Patterns (DAMPs)—endogenous molecules that signal cellular stress and damage—contributes to establishing a self-sustaining inflammatory circuit within the pleural microenvironment that promotes tumor initiation and progression and immune evasion. Among DAMPs, High-Mobility Group Box 1 (HMGB1) has emerged as a key regulator of mesothelioma pathogenesis. Several studies demonstrated that mesothelial cells actively secrete HMGB1 in response to asbestos exposure, driving macrophage recruitment, cytokine production, and chronic inflammation. Beyond HMGB1, additional DAMPs—including IL-33, extracellular ATP, cell-free nucleic acids, heat shock proteins, and calreticulin—contribute to inflammasome activation, stromal remodeling, and immune dysregulation. Recent evidence suggests that DAMP signaling in mesothelioma is dysregulated, resulting in chronic inflammation coupled with ineffective antitumor immunity. This review provides a comprehensive synthesis of DAMP biology in mesothelioma, highlighting the emerging therapeutic opportunities targeting DAMP-associated pathways. Full article

Emphysema is a chronic lung disease characterized by irreversible alveolar destruction, with distinct imaging subtypes—centrilobular emphysema (CLE), panlobular emphysema (PLE), and paraseptal emphysema (PSE). The cellular and molecular mechanisms driving subtype-specific pathogenesis remain poorly understood. Here, we performed single-cell RNA sequencing on emphysematous lung tissues from nine patients (three per subtype) to map the transcriptional landscape across CLE, PLE, and PSE. Profiling 84,704 high-quality cells, we identified eight major cell types, and subsequent subclustering uncovered subtype-enriched populations and transcriptional features. CLE was characterized by upregulated inflammatory pathways in ciliated cells and activated macrophage–epithelial/fibroblast crosstalk, suggesting an airway-derived infection and inflammatory phenotype. In PLE, the proportions of Natural Killer T (NKT) cells and Group 1 innate lymphoid cells (ILC1s) with enhanced cytotoxicity were increased, and mesothelial cells showed upregulation of extracellular matrix (ECM)-related genes, indicating dysfunction in innate immune cells and abnormal repair of mesothelial cells. PSE showed pronounced ECM remodeling signatures, with an increased proportion of systemic venous endothelial cells and enhanced fibroblast–epithelial interactions. Collectively, our findings reveal that CLE is predominantly driven by airway-originated inflammation, PSE exhibits a fibrosis-like remodeling phenotype, and PLE represents an intermediate state of innate immune activation and matrix dysregulation, providing a single-cell resolution framework for subtype-specific therapeutic targeting. Full article

Peritoneal dialysis (PD) is an effective renal replacement therapy; however, its long-term use is limited by the detrimental effects of glucose-based PD fluids on the peritoneal membrane, contributing to fibrosis and ultrafiltration failure. Previous studies have demonstrated that high-glucose exposure promotes oxidative DNA damage through upregulation of thioredoxin-interacting protein (TXNIP) expression, resulting in reduced thioredoxin (Trx) activity. This study investigated strategies to reduce oxidative stress in human peritoneal mesothelial cells exposed to high glucose concentrations. TXNIP expression, Trx activity, intracellular oxidative stress levels, and oxidative DNA damage were analyzed. High-glucose exposure caused a dose-dependent increase in TXNIP expression, a 5–15% reduction in Trx activity, and increased intracellular oxidative stress levels and oxidative DNA damage. Pre-treatment with the ROS scavenger N-acetylcysteine (NAC) reduced these effects. These findings demonstrate that glucose-induced TXNIP upregulation disrupts cellular redox homeostasis, resulting in increased intracellular oxidative stress and oxidative damage. Antioxidant compounds may therefore represent promising therapeutic strategies to protect the peritoneal membrane and improve long-term outcomes in PD. Full article

Ovarian cancer (OC) remains the most lethal gynecological malignancy, mostly due to its frequent diagnosis at advanced stages, early peritoneal dissemination, ascites formation, and limited sensitivity of currently available approaches for early detection. Extracellular vesicles (EVs), particularly exosomes, mediate intercellular communication through the transfer of proteins, lipids, metabolites, and nucleic acids. In OC, EV-associated protein profiles reflect both tumor-cell-intrinsic programs and the complex interactions between malignant cells and the peritoneal microenvironment. This review summarizes current evidence regarding the involvement of exosomal proteins in OC progression, with particular emphasis on epithelial–mesenchymal transition, mesothelial reprogramming, extracellular matrix remodeling, angiogenesis, immune suppression, peritoneal dissemination, and platinum resistance. Mechanistic studies indicate that exosomal proteins, including CD44, the integrin α5β1/asparaginyl endopeptidase complex, annexin A2, low-density lipoprotein receptor-related protein 1, and programmed death-ligand 1, can directly contribute to metastatic niche formation and tumor progression. In parallel, proteomic studies of plasma-, serum-, ascites-, peritoneal-fluid-, and uterine-lavage-derived EVs have identified candidate liquid-biopsy biomarkers, including MUC1, EpCAM, FOLR1, integrins, complement- and coagulation-related proteins, and proteins associated with treatment resistance. To integrate the biological significance of proteins reported in OC-associated exosomes, we additionally performed protein–protein interaction and functional enrichment analyses. These analyses revealed interconnected protein groups associated with cell adhesion, oxidative stress adaptation, secretory remodeling, lipid metabolism, extracellular matrix organization, and inflammatory signaling. Taken together, the available evidence supports exosomal proteome profiling as a promising approach for investigating OC dissemination and developing minimally invasive diagnostic and prognostic tools. However, standardized EV isolation, quantitative proteomics, functional validation, and independent clinical cohorts remain essential for translation into clinical practice. Full article

Background/Objective: The incidence and clinical utility of pleural tissue debris, occasionally encountered in drainage systems, have not been systematically evaluated. We aimed to determine the frequency of tissue debris detection in patients undergoing drainage for pleural effusion, and its utility for the differential diagnosis of exudative effusion and pathological diagnosis of malignant pleural effusion (MPE). Methods: This retrospective proof-of-concept analysis included 325 consecutive patients who underwent percutaneous effusion drainage. The incidence, histopathological findings, and potential predictors of tissue debris were evaluated. For patients with MPE, the adequacy of tissue for immunohistochemistry and molecular testing was evaluated, and the diagnostic sensitivity of tissue debris for MPE was calculated and compared with that of cytology with cell blocks. Results: Tissue debris was detected in 151 patients (46.5%), more frequently in exudates than in transudates (51.7% vs. 23.3%, p < 0.001), and most frequently in patients with MPE (64.6%, p < 0.001). MPE was the only independent predictor of tissue debris detection (adjusted odds ratio 5.74, 95% CI 2.25–9.31). The pathological findings of the debris were classified into metastatic carcinoma/lymphoma (49.0%), acute/chronic inflammation (30.4%), fibrinoid material with inflammation (17.2%), mesothelial reaction (2.6%), and acute suppurative pleuritis/abscess (0.7%). Among the 74 cases with MPE diagnosed using tissue debris, immunohistochemistry and molecular testing were feasible in 85.1% and 69.0% cases, respectively. Diagnostic sensitivity of tissue debris for MPE was significantly higher than that of cytology (77.9% vs. 66.3%; p = 0.035) with a combined sensitivity of 84.2%. Conclusions: Systematic collection of tissue debris, a previously underrecognized clinical specimen obtained during effusion drainage, may be highly valuable for the diagnosis of MPE and adequate for immunohistochemistry and molecular testing, reducing the reliance on invasive biopsy and supporting precise oncological decisions. Full article

We report a rare case of simultaneous well-differentiated papillary mesothelial tumor (WDPMT) and multicystic mesothelioma. The concurrent occurrence of these entities is exceptionally uncommon and may pose challenges during surgical intervention. Both lesions are rare mesothelial proliferations that are often identified incidentally during surgery. Well differentiated papillary mesothelial tumor (WDPMT) is a neoplastic mesothelial proliferation of low malignant potential, which predominantly involves the peritoneum of young women. Microscopically it is composed of branching plump papillae lined by a single layer of bland cuboidal mesothelial cells. Cytologic atypia is minimal, and mitoses usually absent (or at most 1 mitosis per 10 high power fields). Differential diagnosis includes: 1. diffuse malignant peritoneal mesothelioma, 2. localized malignant peritoneal mesothelioma, 3. serous borderline tumors. A 41-year-old patient was admitted for laparoscopic surgery due to a tumor mass localized near the left ovary. Ultrasound examination revealed solid lesion adjacent to the left ovary, exhibiting central vascularization. The patient was diagnosed with the solid tumor mass during routine gynecological examination. The mass was extraovarian and positioned between the left ovary and the uterus. Over the course of the next 18 months, the tumor increased 5 cm in size. Given the fact that the patient presented with no symptoms, such as abdominal pain, distension or ascites, and that the tumor markers were not elevated, additional radiological imaging such as CT or MRI of the abdomen and pelvis was not performed. Intraoperatively, the mass appeared as an extraovarian solid tumor of soft consistency positioned between the left ovary and the uterus. Extirpation of the tumor was performed. Frozen section analysis of the extirpated tumor mass confirmed the diagnosis of WDPMT. During the laparoscopic procedure, a left adnexectomy was also performed and multiple biopsies of white nodules were found dispersed in the peritoneal cavity. Final patohystological analysis concluded that these nodules were peritoneal inclusion cysts. Almost three years after the procedure, the patient is without symptoms and regular clinical and ultrasound examinations were performed every six months, which showed no signs of recurrence or dissemination of the primary tumor. Recognizing well-differentiated papillary mesothelial tumor and multicystic mesothelioma is critical for accurate differential diagnosis from malignant mesothelioma. Awareness of these entities informs appropriate surgical management and follow-up protocols. Full article

Background/Objectives: Standard treatment for ovarian cancer includes surgery and chemotherapy, either as primary “debulking” surgery followed by adjuvant chemotherapy or neoadjuvant chemotherapy followed by interval debulking surgery. The degree of surgical resection correlates with overall survival, with “suboptimal debulking” (visible remaining cancer) being a poor prognostic variable. TGF-β pathway activation is associated with ovarian cancers that cannot be optimally debulked. To test the role of this pathway in ovarian cancer biology, modulation of the pathway was performed in in vitro and in vivo ovarian cancer model systems. Methods: A small molecule TGF-β receptor 1 (TGFBR1) kinase inhibitor, LY2157299, was used to test the in vitro cellular adhesion, proliferation, migration and invasive ability of ovarian cancer cells in culture. A TGF-β responsive reporter construct was used to determine the role of TGF-β pathway in those interactions. To test the effects of TGF-β inhibition in vivo, TGFBR1 and TGFBR2 CRISPR knockout cells were generated and examined for growth and sensitivity to chemotherapy. Results: For ovarian cancer cells responsive to exogenous TGF-β1 treatment, LY2157299-mediated the TGF-β pathway inhibition decreased cell migration and invasion, as well as mesothelial cell to cancer cell adhesion, proliferation, and migration. TGFBR1 and TGFBR2 CRISPR knockout cells showed decreased proliferation baseline or when treated with TGF-β and LY2157299. TGFBR2 CRISPR cells also showed increased sensitivity to cisplatin, with a significant decrease in tumor weight in vivo. Conclusions: TGF-β pathway inhibition successfully targeted many of the cancer cell behaviors that could contribute to suboptimally debulked patients and showed an additive anti-tumor effect in conjunction with cisplatin. LY2157299 treatment is clinically limited due to solubility, but other TGF-β inhibitors could be highly efficacious treatment options. Full article

High-mobility group box 1 (HMGB1) has been implicated in matrix remodeling and fibrotic disorders; however, its role in tuberculosis (TB)-associated pleural fibrosis remains unknown. Pleural fluid levels of HMGB1 and matrix metalloproteinase-1 (MMP-1) in patients with TB pleural effusion (TBPE, n = 36) or transudative pleural effusion (TPE, n = 14) were measured. The effects of Mycobacterium tuberculosis H37Ra (MTBRa) on HMGB1 and MMP-1 expression and their effects on mesothelial–mesenchymal transition (MMT) in human pleural mesothelial cells (PMCs) were assessed. The levels of HMGB1 and MMP-1 were significantly higher in TBPE than in TPE. Elevated HMGB1 and MMP-1 levels in TBPE were positively correlated and both factors were significantly associated with post-TB residual pleural thickening (RPT), particularly in patients with RPT ≥ 10 mm. Colocalized expression of HMGB1 and MMP-1 was also observed in the pleural mesothelium of TBPE patients. MTBRa significantly induced HMGB1 expression in PMCs through activation of the JNK/AP-1 signaling pathway, leading to MMT, enhanced collagen synthesis, and upregulation of MMP-1. Furthermore, silencing of MMP-1 markedly attenuated HMGB1-triggered MMT response. Collectively, HMGB1 promotes pleural fibrogenesis through JNK/AP-1-dependent and MMP-1-mediated MMT, suggesting that targeting the HMGB1/MMP-1 axis may represent a potential therapeutic strategy for TB-related pleural fibrosis. Full article

For decades, peritoneal metastases (PM) have been regarded as a terminal manifestation of advanced malignancies and managed primarily with palliative intent because of limited sensitivity to systemic therapies. Accumulating clinical, molecular, and immunological evidence now supports the view that PM is not merely an anatomic pattern of spread but a distinct metastatic niche with characteristic biological, microenvironmental, and therapeutic features. This review summarizes the major routes of PM development—transcoelomic, lymphatic, and hematologic dissemination—and emphasizes how these pathways converge through shared biological programs. Core mechanisms include epithelial–mesenchymal transition (EMT), adhesion signaling, extracellular matrix remodeling, and tumor–immune cell interactions. A central focus is the peritoneal tumor microenvironment: mesothelial-to-mesenchymal transition, cancer-associated fibroblast activity, adipocyte-derived metabolic support, macrophage polarization, and regulatory T-cell enrichment collectively shape an immunotolerant and treatment-resistant niche on the peritoneal surface. In addition, evidence from pre-metastatic niche biology suggests that primary tumor-derived exosomes and epitranscriptomic regulation can prime the peritoneal environment before overt implantation. These features provide a biological rationale for locoregional strategies such as cytoreductive surgery and hyperthermic intraperitoneal chemotherapy, as well as emerging intraperitoneal modalities and microenvironment-targeted approaches. Finally, organoid platforms, liquid biopsy-based minimal residual disease monitoring, and theranostic technologies may enable more personalized, biology-driven management of PM. Full article

Gastric cancer peritoneal metastasis is not simply an extension of the primary tumor into the abdominal cavity. It represents a biologically distinct disease context shaped by interactions between disseminated tumor cells, peritoneal fluid, mesothelial surfaces, submesothelial stroma, extracellular matrix, immune populations, and malignant ascites. In this narrative review, we examine peritoneal metastasis as a transition between three related but physiologically different states: the primary gastric tumor, free-floating tumor cells or spheroids in the peritoneal fluid, and established mesothelial or submesothelial metastatic implants. We discuss how tumor cells acquire dissemination competence in the primary tumor, survive detachment and fluid-phase stress, adhere to remodeled mesothelium, recruit stromal and immune support, and adapt to ascites-mediated signaling. We also review how the peritoneal niche may contribute to biomarker discordance, immune exclusion, therapeutic resistance, and limitations of conventional response assessment. Where relevant, we distinguish evidence derived directly from gastric cancer peritoneal metastasis from preclinical data, extrapolation from other peritoneal malignancies, and hypothesis-generating interpretation. Finally, we summarize practical implications for tissue sampling, ascites and lavage analysis, biomarker interpretation, translational modeling, and peritoneal-directed therapeutic strategies. A clearer understanding of the biological divergence between the primary tumor, the fluid-phase compartment, and peritoneal implants may improve the study and clinical management of gastric cancer peritoneal metastasis. Full article

Epicardial mesothelium plays a pivotal role in postinfarction cardiac repair by generating fibroblasts, producing extracellular matrix, and releasing paracrine mechanisms. However, interspecies differences have not been sufficiently studied, particularly in in vivo models of scar-free healing such as the African spiny mouse (Acomys cahirinus). This study aimed to compare the profibrotic response of epicardial mesothelial cells (MCs) from Acomys and C57BL/6 mice to hypoxic stress, a key factor in postinfarction recovery. We isolated epicardial MCs from the African spiny mouse (Acomys cahirinus), a species with documented cardiac regenerative capabilities, and from C57BL/6 laboratory mice. Using a CoCl₂-induced hypoxia model in vitro, we assessed cell viability, morphological changes, and expression of epithelial and fibroblast markers. In vivo, following experimental myocardial infarction (MI), we evaluated tissue hypoxia (pimonidazole adducts), epicardial activation (layer thickness, Wt1⁺ and TBX18⁺ progenitor cells), and collagen accumulation. The study was conducted using real-time PCR, Western blotting, immunohistochemical analysis and microscopic examination. In vitro, MCs from both species exhibited an epithelial-like phenotype under normoxic conditions, expressing E-cadherin and cytokeratin 18. Hypoxia (200 µM CoCl₂) induced a comparable response in both Acomys and C57BL/6 cells, characterized by a shift to a spindle-shaped, fibroblast-like morphology, decreased E-cadherin expression, and increased pro-collagen 1 and α-SMA expression. Following MI, both species exhibited similarly extensive hypoxic areas affecting the epicardial zone. Epicardial activation dynamics were comparable: from day 3 post-MI, epicardial thickness increased significantly, and Wt1⁺ and TBX18⁺ progenitor cells accumulated, peaking during the first week. Collagen accumulation in the epicardial region was similar between species, although the number of Wt1⁺ cells was higher in C57BL/6 on day 7. Despite the well-known superior regenerative capacity of spiny mice, epicardial MCs from Acomys and C57BL/6 demonstrated similar signs of profibrotic responses to hypoxic stimulation both in vitro and following MI. These findings suggest that species-specific regenerative outcomes may not be attributable to differential acute epicardial sensitivity to hypoxia, but rather to downstream mechanisms or additional factors influencing the cardiac repair process. This study provides the first characterization of Acomys epicardial MCs and establishes a foundation for further investigation of evolutionarily conserved and species-specific mechanisms of cardiac regeneration. Full article

Malignant mesothelioma is an aggressive cancer with limited therapeutic options, highlighting the need for novel strategies targeting metabolic vulnerabilities. Natural polyphenols have gained attention due to their ability to modulate cellular metabolism and apoptosis-related signaling pathways. In this study, we investigated the combined anticancer effects of quercetin (QUE) and arctigenin (ATG) in human malignant mesothelioma cells. QUE and ATG reduced the viability of MSTO-211H cells in a time-dependent manner, while non-malignant mesothelial MeT-5A cells showed relatively limited sensitivity under the tested conditions. Compared with single treatment, the combination treatment further enhanced growth inhibition, with combination index analysis suggesting a potential synergistic interaction. Co-treatment significantly decreased intracellular ATP levels and increased caspase-3/7 activity, suggesting metabolic stress-associated apoptotic responses. Annexin V analysis confirmed increased apoptotic cell populations following combination treatment. Western blot analysis demonstrated reduced expression of anti-apoptotic proteins Mcl-1 and Bcl-xL, along with increased cleavage of caspase-3 and PARP, consistent with involvement of intrinsic apoptosis-associated signaling pathways. In addition, increased phosphorylation of AMPK and altered expression of mitochondrial oxidative phosphorylation (OXPHOS) complex proteins were associated with potential alterations in mitochondrial respiratory protein expression. Collectively, these findings suggest that QUE and ATG co-treatment is associated with increased apoptotic cell death in malignant mesothelioma cells in association with metabolic stress–related mitochondrial functional alterations. Full article

Background: Recurrence poses a major challenge in epithelial ovarian cancer (EOC), often occurring despite optimal first-line therapy. Dormant cancer cells are believed to play a key role, yet the mechanisms driving their reactivation remain unclear. This study examined whether exosomes released by normal peritoneal mesothelial cells (PMCs) and fibroblasts (PFBs) undergoing iatrogenic senescence after carboplatin and paclitaxel exposure contribute to EOC recurrence. Methods and Results: Senescent PMCs and PFBs secreted markedly more exosomes, identified by CD9, CD63, and CD81, compared with young cells. Exosomes from both cell types more effectively reactivated dormant EOC cells (pEOCs, A2780, OVCAR-3, SKOV-3) than non-exosomal medium constituents. Importantly, senescent PMC-derived exosomes most strongly reactivated pEOCs and SKOV-3, whereas those from senescent PFBs exerted greater effects on pEOCs, OVCAR-3, and SKOV-3. Kinetic studies of exosome internalization revealed that this process was generally more efficient in the presence of exosomes derived from senescent cells compared with those from young donor cells. Compositional analysis revealed distinct profiles between young and senescent exosomes compared in two variants: young PMCs/senescent PMCs and young PFBs/senescent PFBS. Senescent PMC exosomes displayed reduced miR-210-3p, miR-409-3p, and miR-421, alongside elevated MMP1, MMP3, and VEGF, while senescent PFB exosomes showed increased amphiregulin and osteopontin but lower MMP1, MMP3, TIMP1, bFGF, VEGF, and HGF. Functionally, senescent PMC exosomes enhanced pEOC migration, invasion, and spheroid formation, and induced the expression of CCL11 and ABCB1. Senescent PFB exosomes promoted migration and upregulated CCL11, TGF-β1, BIRC5, and CHEK1. Conclusions: These findings suggest that therapy-induced senescence in peritoneal cells may contribute to EOC recurrence by reactivating dormant tumor cells through exosomal signaling. Full article

Peritoneal dialysis (PD) is limited by insufficient phosphate removal, leading to adverse cardiovascular outcomes in patients with chronic kidney disease. To advance the understanding of the molecular mechanisms of peritoneal phosphate transport, RNAseq data of phosphate transporters in four PD-relevant cell lines were analyzed. The expression and localization of the respective proteins were validated by immunostaining in these cells. The transcriptomics of omental arterioles from children on PD were analyzed. In vitro Transwell models of an immortalized mesothelial cell line (MeT-5A) and human umbilical vein endothelial cells (HUVECs) and respective co-cultures were established, enabling quantification of phosphate transport across mesothelial and endothelial monolayers. Sodium phosphonoformate tribasic hexahydrate (PFA) and Tenapanor were used to inhibit transcellular and paracellular transport pathways. Cell viability and integrity markers were measured over the experimental periods. SLC20A1 and SLC20A2 were expressed across all studied cell types, while SLC34A2 and SLC34A3 were mesothelial cell-specific. Omental arterioles of children on low-glucose-degradation-product (GDP) PD showed higher SLC20A1 expression vs. stage 5 chronic kidney disease (CKD5) and healthy controls. Permeability for phosphate was lower across MeT-5A compared with HUVEC monolayers and was not further reduced in co-culture. Inhibitors reduced both transcellular and paracellular transport to 75% in MeT-5A and 65% in co-cultures, while no effects were observed in HUVEC alone, suggesting the mesothelial cell layer as a significant barrier for phosphate transport. Our studies provide first analyses combining findings on molecular phosphate transporters in peritoneal cells and arterioles and introducing a Transwell model for quantitative studies of phosphate kinetics. Full article

Polyserositis is an important clinical feature of Glaesserella parasuis (G. parasuis, GPS) infection in pigs, typically presenting as peritonitis, pleuritis, pericarditis, meningitis, and arthritis, resulting in heavy economic losses in the swine industry. However, the current research on the pathogenesis of infectious peritonitis, particularly that caused by GPS, remains limited, and this condition has long been poorly reported in both clinical practice and research. In this study, we investigated the overall changes in gene expression in porcine peritoneal mesothelial primary cells (PPMCs) following a GPS infection using transcriptomics analysis. A total of 779 differentially expressed genes (DEGs) were identified after 12 h of infecting the PPMCs with GPS, resulting in 253 and 526 genes being upregulated and downregulated, respectively. Additionally, 220 DEGs, mainly involved in the NOD-like receptor signaling pathway, the TNF signaling pathway, and the metabolic pathway, were enriched in the KEGG analysis. These pathways were associated with the main DEGs (IL-1β, IL6, CCL5, CCL2 and NFKBIA), and their gene expression levels were verified through quantitative real-time fluorescence PCR (qRT-PCR). Moreover, oxidative phosphorylation, Salmonella infection, rheumatoid arthritis, and other regulating pathways were clustered together. Our results provide insights into the molecular mechanism underlying GPS-induced peritonitis in swine, identify novel therapeutic targets, and provide research direction for the control and prevention of GPS infections. These insights provide a foundational basis for advancing intervention and prevention approaches for this overlooked yet clinically significant manifestation of polyserositis. Full article